Inflammasome activation in end‐stage heart failure‐associated atrial fibrillation

Aims Inflammatory pathways are increasingly recognized as an important factor in the pathophysiology of both heart failure (HF) and atrial fibrillation (AF). However, there is no data about inflammation‐related histological and molecular alterations in HF‐associated AF. The objective of our study wa...

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Published in:ESC Heart Failure 2022-08, Vol.9 (4), p.2747-2752
Main Authors: Kugler, Szilvia, Onódi, Zsófia, Ruppert, Mihály, Sayour, Alex Ali, Oláh, Attila, Benke, Kálmán, Ferdinandy, Péter, Merkely, Béla, Radovits, Tamás, Varga, Zoltán V.
Format: Article
Language:English
Subjects:
Atrial fibrillation
Body mass index
Cardiac arrhythmia
Cytokines
Diabetes
Ejection fraction
Fibrosis
Heart failure
Infections
Inflammasome
Macrophages
Proteins
Sensors
Short Communication
Short Communications
Sinuses
Software
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Summary:Aims Inflammatory pathways are increasingly recognized as an important factor in the pathophysiology of both heart failure (HF) and atrial fibrillation (AF). However, there is no data about inflammation‐related histological and molecular alterations in HF‐associated AF. The objective of our study was to investigate inflammatory pathways and fibrosis in end‐stage HF‐associated AF. Methods and results Left atrial samples of 24 male patients with end stage ischemic HF undergoing heart transplantation were analysed. Twelve patients suffered from sustained AF while the others had no documented AF. The expression of inflammasome sensors and their downstream signalling were investigated by Western blot. No differences were observed in the expression of inflammasome sensors between the two groups, while cleaved caspase‐1 increased tendentiously in the AF group (P = 0.051). Cleaved caspase‐1 also showed significant correlation with the expression of interleukin‐1β and its cleaved form in the total population and in the AF group (P 
ISSN:2055-5822
2055-5822
DOI:10.1002/ehf2.13972